Abstract
Fetal heart rate (FHR) deceleration is the most common change seen during labor. The role of the autonomic nervous system in regulating the fetal cardiovascular response during multiple uterine contractions has been well-established. However, the mechanism underlying the hemodynamic response remains unclear and the specific reflex that mediates the cardiovascular modifications is still controversial. This study aimed to determine the role of the sympathetic and parasympathetic systems on fetal hemodynamics in complete cord occlusion. Chronically instrumented fetal sheep were randomized to receive an intravenous injection of atropine 2.5 mg (n = 8), propranolol 5 mg (n = 7), atropine and propranolol (n = 7), or a control protocol (n = 9), followed by three episodes of 1-minute umbilical cord occlusion repeated every 5 minutes. Cord compression induces a rapid decrease in the FHR and a rapid increase in MAP. The decrease in FHR is caused by an increase in parasympathetic activity, (atropine and atropine-propranolol abolish the FHR response to the occlusion). The change in FHR during occlusion was not modified by propranolol injection, showing no effect of sympathetic tone. The increase in MAP during occlusion was similar in the four protocols. After releasing occlusion, the FHR was still lower than that at baseline due to a sustained parasympathetic tone. Suppression of the parasympathetic output to the cardiovascular system unmasks an increase in the FHR above baseline values. The lower FHR with the propranolol protocol further supports an increase in myocardial β-adrenoceptor stimulation after cord release. The increase in MAP after cord release was similar in the four protocols, except after the early stage of interocclusion period in atropine protocol. Four minutes after cord release, the FHR returned to baseline irrespective of the drugs that were infused, thereby showing recovery of ANS control. Blood gases (pH, PaCO2, PaO2) and plasma lactate concentrations was similar between the four protocols at the end of three applications of UCO. Complete cord compression-induced deceleration is likely due to acute activation of parasympathetic output. β-adrenoceptor activity is involved in the increase in FHR after cord release. Understanding the reflexes involved in FHR deceleration may help us understand the mechanisms underlying fetal autonomic adaptation during cord occlusion.
Highlights
During labor, fetal heart rate (FHR) recordings are the only non-invasive tool that can continuously monitor intrapartum fetal well-being
After drug injections and before umbilical cord occlusion (UCO), FHR was higher with the atropine protocol than with the control protocol, and lower with the propranolol protocol than with the control protocol (p
Deceleration of FHR is common during labor and reflects fetal compensation in response to hypoxia during uterine contractions [2]
Summary
Fetal heart rate (FHR) recordings are the only non-invasive tool that can continuously monitor intrapartum fetal well-being. Knowledge and understanding of fetal physiology are required to interpret FHR recordings, [1,2]. Decelerations associated with uterine contractions are the most common and distinctive component of intrapartum FHR [3,4]. The role of the autonomic nervous system (ANS) in regulating FHR and mean arterial pressure (MAP) during uterine contractions to maintain optimal organ perfusion is well-established [3,5,6]. The parasympathetic output and sympathetic output at different time points during and after FHR deceleration remain incompletely understood [3,7,8]. A better understanding of the sequence of ANS activity during FHR may help decipher which reflexes trigger FHR decelerations [9]
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